Investigation of apoptotic effects of D-pantothenic acid on PC-3 prostate cancer cells

Yıl 2020, Cilt: 45 Sayı: 4, 1499 - 1504, 27.12.2020

Ares Alizade , Gülüzar Özbolat

https://doi.org/10.17826/cumj.736494

Öz

Purpose: The anti-inflammatory and antioxidant properties of D-pantothenic acid have been demonstrated and the effects of dexpentanol on inflammatory pathways and apopototic pathways that trigger cell death are of interest. Apoptotic pathways are important in resistance to chemotherapeutics in cancer diseases and in cancer development. Therefore, we planned how treatment of PC-3 human prostate cancer cells with dexpanthenol will affect the levels and activities of apoptotic and inflammation mediators. For this purpose, human prostate cancer cell culture was performed.
Materials and Methods: The human prostate cancer cells were treated with dexpentanaol then protein levels and activities of inflammatory and apoptotic pathway mediators such as gadd153, AIF, grp78, bax and bcl-2 in the cells were analyzed by ELISA.
Results: The results of our study showed that, D-pantothenic acid did not statisticaly decreased the leves of bax, bcl-2 and grp78 protein expression in PC-3 prostate cancer cells. The effect of D-pantothenic acid on gadd153 and AIF proteins in PC-3 cells was increased but this increased level did not statisticaly significant.
Conclusion: Recent studies have demonstrated the potential benefits of anti-inflammatory drugs. Our study showed that D-pantothenic acid had no significant effect on the growth of PC-3 cells and has no significant effect on intracellular apoptotic pathways.

Destekleyen Kurum

This study was funded by Mustafa Kemal University Research Projects Unit (Project no:18.M.096).

Proje Numarası

This study was funded by Mustafa Kemal University Research Projects Unit (Project no:18.M.096).

Teşekkür

This study was funded by Mustafa Kemal University Research Projects Unit (Project no:18.M.096).

D-pantotenik asidin PC-3 prostat kanseri hücreleri üzerindeki apoptotik etkilerinin incelenmesi

Öz

Amaç: D-pantotenik asidin anti-enflamatuar ve antioksidan özellikleri gösterilmiştir ve dekspentanolün hücre ölümünü tetikleyen enflamatuar yolaklar ve apopototik yollakar üzerindeki etkileri, merak uyandırmaktadır. Apoptotik yolaklar, kanser hastalıklarında ve kanser gelişiminde kemoterapötiklere karşı dirençlilik açısından önemlidir. Bu nedenle, PC-3 insan prostat kanseri hücrelerinin dekspantenol ile tedavisinde apoptotik ve inflamasyon mediyatörlerinin seviyelerini ve aktivitelerini nasıl etkileyeceğini planladık. Bu amaçla, insan prostat kanseri hücre kültürü yapıldı.
Gereç ve Yöntem: İnsan prostat kanseri hücreleri, dekspentanaol ile muamele edildi ve hücrelerde gadd153, AIF, grp78, bax ve bcl-2 gibi enflamatuar ve apoptotik yolaklardaki aracıların protein seviyeleri ve aktiviteleri ELISA ile analiz edildi.
Bulgular: Çalışmamızın sonuçları, D-pantotenik asidin PC-3 prostat kanseri hücrelerinde bax, bcl-2 ve grp78 protein ekspresyonu düzeylerini istatistiksel olarak azaltmadığını gösterdi. PC-3 hücrelerinde D-pantotenik asidin üzerindeki etkisi, gadd153 ve AIF proteinleri arttırıldığı, ancak bu artış seviyesi istatistiksel olarak anlamlı değildi.
Sonuç: Son çalışmalar, anti-enflamatuar ilaçların potansiyel faydalarını göstermiştir. Çalışmamız D-pantotenik asidin PC-3 hücrelerinin büyümesi ve hücre içi apoptotik yolaklar üzerinde anlamlı bir etkisinin olmadığını göstermiştir.

Anahtar Kelimeler

D-pantothenic acid, dexpanthenol, prostat kanseri

Proje Numarası

This study was funded by Mustafa Kemal University Research Projects Unit (Project no:18.M.096).

Kaynakça

• 1. Aydın S, Boz MY. Türkiye’de üriner sistem kanserlerinin görülme sıklığında hızlı değişme. Turk Urol Derg. 2015;41(4):215–20.
• 2. Jemal A, Siegel R, Ward E, Hao Y, Xu J, Murray T, et al. Cancer Statistics, 2008. CA Cancer J Clin [Internet]. 2008;58(2):71–96.
• 3. Stephenson RA. Prostate cancer overdiagnosis and over treatment.Analysis of US mortality and SEER incidence. Trends in thePSA and pre-PSA eras. In Klein EA (ed): Management of ProstateCancer, 2 nd ed. Totowa, NJ, Humana Pres. 2004:3-13.
• 4. Anderson J. Treatment of prostate cancer-The role of primaryhormonal therapy. EAU Update series. 2003:1;32-9
• 5. Hellerstedt BA, Pienta KJ. The current state of hormonal therapy for prostate cancer. CA Cancer J Clin. 2002:52;154-79.
• 6. Daskivich TJ, Oh WK. Recent progress in hormonal therapy for advanced prostate cancer. Curr Opin Urol. 2006:16;173-8.
• 7. Abrahamsson P. Revalutions in the management of hormone refractory prostate cancer. Eur Urol Suppl 2003:2;1-2.
• 8. Gleave M, Kelly WK. High-risk localized prostate cancer: acase for early chemotherapy. J Clin Oncol. 2005:23;8186-91.
• 9. Peppa M, Uribarri J., Vlassara H. Glucose, advanced glycation end products, and diabetes complications: what is new and what works Clin. Diabetes, 21 (4) (2003), pp. 186--187
• 10. Bucciarelli L.G., Wendt T., Rong L., et al. RAGE is a multiligand receptor of the immunoglobulin superfamily: implications for homeostasis and chronic disease Cell Mol. Life Sci., 59 (7) (2002), pp. 1117—1128
• 11. Alizadehshargh S, Güner-Akdoğan G. Apopitoz: düzenleyici moleküller, hastalıklarla ilişkisi ve apopitozu saptama yöntemleri. Turkiye Klinikleri J Med Sci 2009;29:1677-86. 72.
• 12. Tomatır AG. Apoptosis: programmed cell death. Turkiye Klinikleri J Med Sci 2003;23:499-508.
• 13. Cline AM, Radic MZ. Apoptosis, subcellular particles, and autoimmunity. Clin Immunol. 2004;112(2):175-82.
• 14. Çıtak EÇ. Apoptosis and cancer. Turkiye Klinikleri J Pediatr 2000;9(3):183-91. 36.
• 15. Call JA, Eckhardt SG, Camidge DR. Targeted manipulation of apoptosis in cancer treatment. Lancet Oncol 2008;9(10):1002-11
• 16. Yılmaz HH, Yazıhan N, Tunca D, Sevinç A, Olcayto EÖ, Özgül N, et al. Cancer trends and incidence and mortality patterns in Turkey. Japanese journal of clinical oncology. 2010:hyq075. 5. Society, Society AC.
• 17. Zeegers M, Jellema A, Ostrer H. Empiric risk of prostate carcinoma for relatives of patients with prostate carcinoma. Cancer. 2003; 97(8):1894-903
• 18. Wang Z, Li Y, Banerjee S, Sarkar FH. Exploitation of the Notch signaling pathway as a novel target for cancer therapy. Anticancer research 2008;28: 3621-3630.
• 19. Wang Z, Zhang Y, Li Y, Banerjee S, Liao J, Sarkar FH. Down-regulation of Notch-1 contributes to cell growth inhibition and apoptosis in pancreatic cancer cells. Molecular cancer therapeutics 2006;5: 483-493.